Diabetes Mellitis N/c

Front 1

What is diabetes mellitis?

Back 1

Hyperglycemia! due to ↓ insulin synthesis (DM1) or ↑ insulin resistance (defect in insulin receptors at target tissue) (DM2)

Front 2

CP of DM?

Back 2

1. Polyuria ( ↑ urination)
2. Polydypsia ( ↑ thirst)
3. Microvascular disease
4. Macrovascular disease

Front 3

What are the major microvascular diseases in DM (3)?

Back 3

1. Retinopathy
2. Nephropathy
3. Peripheral neuropathy

Front 4

What senses lost in peripheral neuropathy? Describe distribution of peripheral neuropathy?

Back 4

Vibration & pain sense lost in a stocking distribution

Front 5

What are patients at risk for due to peripheral neuropathy?

Back 5

ulcers!

What type of infection are people w/ DM susceptible to?= fungal infections (especially candida albicans)

Front 6

What are the 3 ways that retinopathy in DM can present? Hallmarks of each?

Back 6

1. Nonproliferative -- aneurysms & hemorrhage
2. proliferative -- neovascularization
3. macular edema -- retinal thickening towards macula

Front 7

What are the major macrovascular disease in DM (3)?

Back 7

1. Atherosclerosis
2. CHD
3. Stroke

Front 8

Important to regularly screen for what 3 things to monitor DM progression?How?

Back 8

1. Foot for periphera; neuropathy
2. Retina for retinopathy
3. Nephropathy

Front 9

How do you dx DM? Criteria for dx?

Back 9

glycosylated HbA1c → >6.5%

Front 10

Why is HbA1c better than glucose directly? How does it measure preceding months?

Back 10

gives you glucose levels in 1-3 preceding months. Measures lifetime of Hb.

Front 11

What are the 2 types of DM? Pathological hallmark & pathogenesis of each?

Back 11

DM1 -- auto-antibodies destroy b-cells → ↓ insulin synthesis!
DM2 -- ↓ insulin receptors at target tissue → insulin resistance

Front 12

Pathohistological hallmark of DM1?

Back 12

insulitis! → inflammation and destruction of b-cells

Front 13

For the following, describe DM1 vs DM2

Back 13

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Front 14

Age of onset?

Back 14

DM1 -- <20 → juvenille onset
DM2 -- >30 → adult onset

Front 15

Family history?

Back 15

DM1 -- No
DM2 -- Yes

Front 16

Body shape?

Back 16

DM1 -- thin
DM2 -- fat

Front 17

Major devastating complication?

Back 17

DM1 -- Diabetic keotacidosis (DKA)
DM2 -- Hyperosmolar Hyperglycemic state

Front 18

Diabetic Ketoacidosis (DKA)

Back 18

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Front 19

DKA is a major complication of which DM?

Back 19

DM1

Pathogenesis of DKA? = ↓ insulin → lipolysis → fatty acids → ketogenesis of fatty acids in liver → ketoacidosis

Front 20

How is insulin deficiency perpetuated by DKA?

Back 20

vomiting due to DKA → ↑ counterregulatory hormones (catecholamines, GH, Cortisol) → ↓ insulin

Front 21

Why does DKA not occur in DM2?

Back 21

No ↓ insulin!

Front 22

Hallmarks of DKA (2)?

Back 22

1. Ketoacidosis!
2. Hyperglycemia → osmotic dieuresis

Front 23

3 diagnostic features of DKA?

Back 23

1. ↑ anion gap
2. ↓ resp min volume
3. Osmotic diuresis

Front 24

How does anion gap ↑?

Back 24

use up CO2 b/c acidosis

Front 25

What is osmotic diuresis? How does it lead to intracellular dehydration?

Back 25

hyperglycemia → ↑ [glucose] in urine → ↑ ECF urinated out → water travels from intracellular to extracellular space!

Front 26

What are the 2 major clinical syndromes that result from too much fluid loss?

Back 26

hypernatremia, hyperkalemia

Front 27

What does respiratory min volume indirectly measure? How does a ↓ in RMV occur?

Back 27

total CO2.

Acidosis → ↓ CO2 → ↓ RMV

Front 28

Clinical presentation? Each is caused by what underlying pathology?

Back 28

1. Tachycardia, hypotension -- osmotic dieuresis
2. Nausea, abdominal pain & vomiting! -- ketoacidosis
3. Kussmaul respiration (rapid, deep breathing) -- ketoacidosis
4. Coma

Front 29

How do you tx DKA?

Back 29

1. tx underlying conditions like Hypernatremia & hyperkalemia
2. Insulin! regardless of blood glucose level

Front 30

What is absolutely required for resolution of DKA?

Back 30

insulin

Front 31

What 2 CP is unique to DKA not HHS?

Back 31

1. Kussmaul respiration
2. Vomiting

Front 32

Hyperosmolar hyperglycemic state (HHS)

Back 32

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Front 33

HHS is a major emergency of which DM?

Back 33

DM2

Front 34

Pathogenesis of HHS?

Back 34

Hyperglycemia → osmotic diueresis → intracellular dehydration

Front 35

Hallmarks of HHS (2)?

Back 35

1. Hyperglycemia (much > than DKA)
2. Hyperosmolarity!

Front 36

What pathology is missing in HHS that makes a huge diff from DKA?

Back 36

ketoacidosis

Front 37

CP of HHS?

Back 37

similar to DKA

Front 38

What is notably missing from CP as opposed to DKA?

Back 38

vomiting & kussmaul respiration

Front 39

Tx of HHS?

Back 39

1. Fluid intake
2. Insulin

Front 40

What happens as a result of ↓ serum glucose?

Back 40

water travels from extracellular to intracellular space

Front 41

What is a major complication if ↓ glucose too fast?

Back 41

cerebral edema!

Front 42

Treatment of DM

Back 42

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Front 43

What is the main therapeutic goal of DM? Why?

Back 43

Glycemic control (diet, exercise & insulin) → to minimize microvascular & macrovascular complications

Front 44

What is quantifiable goal of DM tx?

Back 44

HbA1C < 7%

In addition to glycemic control, what else is used to ↓ macrovascular risks?= smoking cessation, BP control, & lipid control

Front 45

Tx DM1 vs DM2?

Back 45

DM1 -- Glycemic control w/ diet, exercise, monitor intake, insulin
Basal-bolus insulin

DM2 -- Glycemic control w/ diet, exercise, monitor intake, insulin +
1. Oral non-insulin
2. Injectiable non-insulin

Front 46

What are the non-insulin oral tx? (5)

Back 46

1. Sulfonylurea
2. Biguanides (metformin)
3. TZDs
3. A-glucosidase inhibitors
4. Bromocriptine
5. DPP inhibitor

Front 47

What are the non-insulin injection tx? (2)

Back 47

1. Exenatide
2. Pramlintide

Front 48

What are the 2 major side effect concerns of non-insulin tx?

Back 48

1. hypoglycemia
2. Weight gain

Front 49

SoA & MoA for each non-insulin tx

Back 49

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Front 50

Biguanides (metformin)

Back 50

Liver → ↑ insulin sensitivity

Front 51

Sulfnonylurea

Back 51

Pancreas → ↑ insulin secretion

Front 52

TZDs

Back 52

GI → ↑ glucose uptake

Front 53

A-glucosidase inhibitors

Back 53

GI → ↓ carbohydrate absorption

Front 54

Bromocriptine

Back 54

DA agonist → ↑ peripheral fuel metabolism

Front 55

DPP inhibitor

Back 55

inhibit DPP-4 → ↑ activity of GLP-1 → ↑ sulon, ↓ glucagon

Front 56

Exenatide

Back 56

mimics GLP-1 but resistant to DPP

Front 57

Pramlintide

Back 57

amylin analog (amylin ↓ postmeal glucagon surge)

Front 58

Insulin

Back 58

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Front 59

What is the problem w/ providing human insulin?

Back 59

high solubility so low bioavailability

Front 60

How are insulin properties synthetically altered?

Back 60

changing aa

Front 61

What are the short-acting synthetic insulin? (3)

Back 61

1. lyspro
2. AspArt
3. Glulysine

Front 62

When are short-acting synthetic insulin used?

Back 62

pre & post meal for burst of insulin

Front 63

What are the long lasting synthetic insulin? (2)

Back 63

1. Detemir
2. Glargine

Front 64

Why are the long lasting synthetic insulin used?

Back 64

maintain basal levels of insulin

Front 65

Insulin schedule scheme for Type 1 DM?

Back 65

Basal-bolus (~ injections/ day → basal, 2 bolus pre & post meal)

Front 66

How do you provide insulin to type 2DM?

Back 66

< complicated, ~1-2 injections/day